ArticleProceedings of the National Academy of Sciences of the United States of America2014
EBV microRNA BART 18-5p targets MAP3K2 to facilitate persistence in vivo by inhibiting viral replication in B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 66 citations in OpenAlex.
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- Epstein-Barr virus and human MiRNAs crosstalk: orchestrating latency, lytic cycle, and immune system modulation.Folia microbiologica · 2026Review
- Profiling miRNA changes in Epstein-Barr virus lytic infection identifies a function for BZLF1 in upregulating miRNAs from the DLK1-DIO3 locus.PLoS pathogens · 2025Article
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- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Implications of EBV-Encoded and EBV-Related miRNAs in Tumors.Current gene therapy · 2025Review
- Alzheimer's disease and infectious agents: a comprehensive review of pathogenic mechanisms and microRNA roles.Frontiers in neuroscience · 2024Review
- Identifying the key regulators orchestrating Epstein-Barr virus reactivation.Frontiers in microbiology · 2024Review
- MicroRNAs in infectious diseases: potential diagnostic biomarkers and therapeutic targets.Clinical microbiology reviews · 2023Review
- Epstein-Barr virus infection: the micro and macro worlds.Virology journal · 2023Review
- Viral miRNA regulation of host gene expression.Seminars in cell & developmental biology · 2023Review
- Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis.PloS one · 2023Article
- Small non-coding RNAs encoded by RNA viruses: old controversies and new lessons from the COVID-19 pandemic.Frontiers in genetics · 2023Review
- MicroRNA Regulation of Human Herpesvirus Latency.Viruses · 2022Review
- Epstein-Barr Virus miR-BHRF1-3 Targets the BZLF1 3'UTR and Regulates the Lytic Cycle.Journal of virology · 2022Article
- Epstein-Barr virus microRNA BART10-3p promotes dedifferentiation and proliferation of nasopharyngeal carcinoma by targeting ALK7.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- EpsteinZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
- Deletion of Viral microRNAs in the Oncogenesis of Epstein-Barr Virus-Associated Lymphoma.Frontiers in microbiology · 2021Review
- Immune Escape by Non-coding RNAs of the Epstein Barr Virus.Frontiers in microbiology · 2021Review
- EBV-encoded miRNAs can sensitize nasopharyngeal carcinoma to chemotherapeutic drugs by targeting BRCA1.Journal of cellular and molecular medicine · 2020Article
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2 authors at 1 institution in 1 country.
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Abstract
EBV is an oncogenic human herpesvirus that has the ability to infect and transform B cells latently in vitro. However, the virus also establishes a lifetime, benign, persistent latent infection in resting memory B cells in vivo, where the virus is quiescent (i.e., expresses none of the known latent proteins). The virus encodes ∼40 micro-RNAs (miRNAs), most of which are transcribed from the BamH1 fragment A rightward transcript (BART) region of the virus. We have shown previously that a subset of these miRNAs is present at high copy numbers in latently infected memory B cells in vivo, suggesting a role in maintaining latency. Here, we describe the role of one of these miRNAs, BART 18-5p. We show that it targets the 3'UTR of the mRNA, encoding the important cellular signaling molecule MAP kinase kinase kinase 2 (MAP3K2), at exactly the same site as the oncogenic cellular miRNA mir-26a-5p. To our knowledge, this is the first report of a virus encoding a miRNA that suppresses a target in the MAP kinase signaling cascade, a central signal transduction pathway that governs a broad spectrum of biological processes. We further show that MAP3K2 is an intermediary in the signaling pathways that initiate lytic viral replication. Thus, 18-5p expression in latently infected B cells has the effect of blocking viral replication. We propose that the role of 18-5p is to maintain latency by reducing the risk of fortuitous reactivation of the virus in latently infected memory B cells.
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